Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The transcriptomic landscape of multiple organs in CHIKV-infected Rhesus monkeys and mice

ABSTRACT: Chikungunya virus (CHIKV) is a mosquito-borne alphavirus that has emerged as a significant public health concern due to its ability to cause severe arthralgia and occasionally fatal cases. The virus has been shown to infect a wide range of tissues, including the heart, liver, spleen, lungs, kidneys, and brain, leading to a spectrum of clinical manifestations.This study aims to investigate the impact of CHIKV infection on the transcriptome of various organs in rhesus monkeys and mice, providing insights into the molecular mechanisms underlying the pathogenesis of CHIKV in different host species.The transcriptome analysis revealed significant alterations in gene expression across the infected tissues in both species.

ORGANISM(S): Mus musculus Macaca mulatta

PROVIDER: GSE262358 | GEO | 2024/06/01

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

the proteomic data of systematic organs of CHIKV-infected mouse and rhesus monkey

Project description:this proteomic data is compromised of 72 samples from 6 mouses and 6 rhesus monkeys. CHIKV, as a mosquito-based virus, is well known to pose threat to muscles and joints, with its symptoms being called chikunkunya fever, whereas its impact on other organs after infection is not completely understood. So we attempt to investigate whether it will cause damage to other organs with infected heart, liver, spleen, lung, kidney, and brain being study object.

2024-05-31 | PXD048726 | Pride

Quantitative proteomic analysis of chikungunya virus-infected Aedes aegypti reveals proteome modulations indicative of persistent infection

Project description:The mosquito-borne chikungunya virus (CHIKV) poses a threat to human health in tropical countries throughout the world. The molecular interactions of CHIKV with its mosquito vector, Aedes aegypti are not fully understood. Following oral acquisition of CHIKV via salinemeals, we analyzed changes in the proteome of Ae. aegypti in 12 h intervals by label-free timsTOF Pro mass spectrometry. For each of the seven time points, between 2647 and 3167 proteins were identified among CHIKV infected and non-infected mosquito samples and fewer than 6% of those identified proteins were affected by the virus.

2020-03-18 | MSV000085115 | MassIVE

Insect-Specific Chimeric Viruses Potentiated Antiviral Responses and Inhibited Pathogenic Alphavirus Growth in Mosquito Cells

Project description:Most alphaviruses are transmitted by mosquito vectors and infect a wide range of vertebrate hosts, with a few exceptions. Eilat virus (EILV) in this genus is characterized by a host range restricted to mosquitoes. Its chimeric viruses have been developed as safe and effective vaccine candidates and diagnostic tools. Here, we investigated the interactions between these insect-specific viruses (ISVs) and mosquito cells, unveiling their potential roles in determining vector competence and arbovirus transmission. By RNA sequencing, we found that these ISVs profoundly modified host cell gene expression profiles. Two EILV-based chimeras, consisting of EILV’s nonstructural genes and the structural genes of Chikungunya virus (CHIKV) or Venezuelan equine encephalitis virus (VEEV), namely EILV/CHIKV (E/C) and EILV/VEEV (E/V), induced more intensive transcriptome regulation than parental EILV and activated different antiviral mechanisms in host cells. We demonstrated that E/C robustly promoted antimicrobial peptide production and E/V strongly upregulated the RNA interference pathway components. This also highlighted the intrinsic divergences between CHIKV and VEEV, representatives of the Old World and New World alphaviruses. In contrast, EILV triggered a limited antiviral response. We further showed that initial chimera infections efficiently inhibited subsequent pathogenic alphavirus replication, especially in the case of E/V infection, which almost prevented VEEV and Sindbis virus (SINV) superinfections. Altogether our study provided valuable information on developing ISVs as biological control agents.

2023-01-19 | GSE220562 | GEO

Interacting Partners of CHIKV nsP3 in Human Macrophages

Project description:Chikungunya virus (CHIKV), an alphavirus transmitted by mosquitoes, has instigated several epidemics in recent years, sparking intensive efforts to understand its biology. Despite progress, the understanding of CHIKV’s molecular interactions with host cell constituents, especially in susceptible cells such as macrophages remain limited. We used mass spectrometry platform to characterize the interactions between CHIKV-nsP3, a viral nonstructural protein, and proteins in human THP-1 macrophage cells. Our findings revealed 196 high-confidence interactions primarily involving nsP3. Further the sub-cellular localization, pathways these interacting proteins might be involved in were deduced using computational methods. The interacting partners were further incorporated into a comprehensive host virus interaction network derived from extensive literature on alphavirus-host interactions. Collectively, this study offers the first interaction map between CHIKV nsP3 protein and THP-1 cells, illuminating new probable roles of host cell proteins in CHIKV’s replication cycle.

2024-03-06 | PXD045252 | Pride

A commensal Clostridium bacteria restricts alphavirus dissemination through a bile acid-type I IFN signaling axis

Project description:The emerging alphavirus chikungunya virus (CHIKV) has infected millions of people. However, the factors modulating disease outcome remain poorly understood. We show that depletion of the gut microbiota in oral antibiotic-treated or germ-free mice leads to greater CHIKV infection and spread within one day of virus inoculation. Perturbation of the gut microbiota alters TLR7-MyD88 signaling in plasmacytoid dendritic cells (pDCs) and blunts systemic production of type I interferon (IFN). Consequently, circulating monocytes express fewer IFN-stimulated genes and become permissive for CHIKV infection. Reconstitution with a single commensal bacterial species, Clostridium scindens, or its derived metabolite, the bile acid deoxycholic acid, can restore pDC- and MyD88-dependent type I IFN responses to restrict systemic CHIKV infection and transmission back to vector mosquitoes. Thus, commensal gut bacteria modulate antiviral immunity and levels of circulating alphaviruses within hours of infection through a bile acid-pDC-IFN signaling axis, which affects virus dissemination and potentially, epidemic spread

2020-05-13 | GSE150387 | GEO

A commensal Clostridium bacteria restricts alphavirus dissemination through a bile acid-type I IFN signaling axis

2020-06-09 | GSE152043 | GEO

Virus-induced codon-specific reprogramming to favor viral RNA translation

Project description:How viruses, such as the emerging mosquito-borne Chikungunya virus (CHIKV), express their genomes at high levels despite an enrichment in suboptimal codons remains a puzzling question. By integrating subcellular fractionation and transcriptome-wide analyses of translation in CHIKV-infected human cells, we demonstrate an unanticipated virus-induced reprogramming of the host translation machinery to favor translation of viral RNA over cellular genes featuring optimal codon usage. This reprogramming was specifically apparent at the endoplasmic reticulum (ER), the preferred translation compartment of CHIKV RNA, and it is mediated by the wobble uridine 34 tRNA modification enzyme KIAA1456 whose expression is enhanced upon viral infection. Since KIAA1456 itself is encoded by a CHIKV-like codon usage, infection triggers a positive feed-back loop that ensures efficient virus protein production. Our findings demonstrate an unprecedented interplay of viruses with the host tRNA epitranscriptome to favor viral protein expression.

2022-06-17 | GSE143390 | GEO

Pathogenesis of chikungunya virus infection associated with fatal outcome

Project description:Chikungunya virus (CHIKV) is a mosquito-borne virus that causes acute, subacute, and chronic human diseases and can cause neurological complications and death. Here, we combined epidemiological, virological, histopathological, cytokine, molecular dynamics, metabolomics, proteomics, and genomic analyses to investigate viral and pathophysiologic factors that contribute to deaths caused by chikungunya (CHIK). Our results indicate that CHIK-deaths presented multiple organs infection, central nervous system damage, and exhibited significantly elevated serum levels of pro-inflammatory cytokines and chemokines compared to survivors. The histopathology, metabolite, and proteomic signatures of CHIK-deaths revealed hemodynamic disorders and dysregulated immune system response. CHIKV East-Central-South-African lineage caused fatal and survivor cases, and CHIKV crosses the blood–brain barrier without tight junction alterations. IFN-λ3 was highly expressed in fatal cases but did not present a direct antiviral effect on CHIKV replication in vitro. In summary, our results reveal insights to improve understanding of CHIK pathogenesis, especially the pathophysiology of fatal infections.

2024-06-16 | PXD043815 | Pride

Transcriptome analysis of Huh7 cells upon Chikungunya virus infection and capsid transfection reveals regulation of distinct cellular and metabolic pathways

Project description:The purpose of this study is to compare the gene profiles of chikungunya virus (CHIKV) capsid transfected and CHIKV infected Huh7 cells to identify the genes differentially expressed in the presence of the capsid protein during CHIKV infection

2021-03-16 | GSE168910 | GEO

Aedes aegypti Aag-2 cells proteome modulation in response to Chikungunya virus infection

Project description:Chikungunya virus (CHIKV) is a single-stranded positive RNA virus that belongs to the genus Alphavirus and is transmitted to humans by infected Aedes aegypti and Aedes albopictus bites. In humans, CHIKV can cause painful symptoms during acute and chronic stages of infection. However, the virus-vector interaction has characteristics that allow a persistent infection, not disturbing the mosquito’s fitness. Here, we aimed to clarify aspects of CHIKV infection in Ae. aegypti Aag-2 cells through label-free quantitative proteomic analysis and transmission electron microscopy (TEM). We used MOI 0.1 to infect Aag-2 cells in biological triplicates over 48 h. TEM images show a high load of intracellular viral cargo at 48 hpi, as well as an elongated unusual mitochondria morphology that might indicate a mitochondrial imbalance. Moreover, a total of 196 Ae. aegypti protein groups were up or downregulated upon infection, related to protein synthesis, energy metabolism, signaling pathways and apoptosis. These regulated Aag-2 proteins might have roles in antiviral and/or in pro-viral mechanisms during CHIKV infection, to support the balance between viral propagation and the survival of host cell, leading to the persistent infection.

2022-06-02 | PXD033231 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data